The abrogation of the PRC2 activity may explain the high levels of MYCN expression in cth+ ETP-ALL [36] as observed in T-ALL cell lines, where induced EZH2 inactivation correlates with an immature signature, transcriptional up-regulation of MYCN, and an increased MYCN-driven replication stress [37]. This evidence concerns the gene EZH2 and acute lymphoblastic leukemia.